Abstract

The interaction between cancer and the organ microenvironment is complex, and the transforming growth factor-β (TGF-β)/Smad pathway plays an important role in this interaction. However, the role of the organ microenvironment in hepatocellular carcinoma (HCC) is not well understood. To evaluate the effect of the organ microenvironment and the role of the TGF-β/Smad pathway, MHCC97-H cells were inoculated subcutaneously into nude mice and the resulting MHCC97-H subcutaneous tumor tissues were implanted into the livers of the mice. We found a higher tumor weight and less pulmonary metastasis for the cancers in liver sites than for those in subcutaneous sites; the TGF-β1 levels were significantly different between the tumor models and correlated with tumor metastasis. Our results suggest that the organ microenvironment affects the growth and invasion of liver cancer cells. The TGF-β/Smad pathway is significant in the interaction between HCC and its microenvironment and affects the progression of HCC.

Highlights

  • Hepatocellular carcinoma (HCC) is one of the most common types of cancer in the world and a significant cause of mortality in sub-Saharan Africa and Eastern Asia [1]

  • These results suggest that the organ microenvironment may alter the invasive potential of HCC

  • We found that the expression levels of TGF-β1 in the MHCC97-H and xenograft models were statistically different

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Summary

Introduction

Hepatocellular carcinoma (HCC) is one of the most common types of cancer in the world and a significant cause of mortality in sub-Saharan Africa and Eastern Asia [1]. The overall five‐year survival rate following resection has remained as low as 35-50% [2,3,4]. The extremely poor prognosis of HCC is largely the result of a high rate of recurrence following surgery and of metastasis [5,6]. Exploring the mechanisms involved in the process of HCC metastasis is vital as it may provide new therapeutic targets for HCC and is likely to be useful in further improving the long-term survival of patients with HCC [7]. TGF-β is able to stimulate non-invasive HCC cells to acquire invasive phenotypes [16] and induces in vitro apoptosis of hepatoma cells [17]

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